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Literature summary for 3.4.21.73 extracted from

  • Schroetzlmair, F.; Kopitz, C.; Halbgewachs, B.; Lu, F.; Alguel, H.; Bruenner, N.; Gaensbacher, B.; Krueger, A.
    Tissue inhibitor of metalloproteinases-1-induced scattered liver metastasis is mediated by host-derived urokinase-type plasminogen activator (2010), J. Cell. Mol. Med., 14, 2760-2770.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.21.73

Application

Application Comment Organism
medicine co-operation between TIMP-1 and host uPA suggests that therapies, simultaneously interfering with pro- and anti-proteolytic pathways may be beneficial for patients with metastatic disease Mus musculus
medicine co-operation between TIMP-1 and host uPA suggests that therapies, simultaneously interfering with pro- and anti-proteolytic pathways may be beneficial for patients with metastatic disease Homo sapiens

Protein Variants

Protein Variants Comment Organism
additional information expression of recombinant human uPA in enzyme-ablated mouse livers using adenoviral transfection Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-
Mus musculus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
liver
-
 Mus musculus
-

Synonyms

Synonyms Comment Organism
uPA
-
 Mus musculus
uPA
-
 Homo sapiens
Urokinase-type plasminogen activator
-
 Mus musculus
Urokinase-type plasminogen activator
-
 Homo sapiens

Expression

Organism Comment Expression
Mus musculus elevated levels of tissue inhibitor of metalloproteinases-1 , TIMP-1, render the liver more susceptible to metastasis by triggering urokinase plasminogen activator expression as well as hepatocyte growth factor signalling, thereby leading to the fatal scattered infiltration of metastasizing tumour cells throughout the parenchyma of the target organ up

General Information

General Information Comment Organism
malfunction livers of uPA-ablated mice elevated TIMP-1 levels do not trigger HGF signalling and do not promote metastasis of a murine T-lymphoma cell line, decreased TIMP-1-induced tumour cell scattering in uPA knockout mice. In contrast, lack of tumour cell-derived uPA induced by gene silencing do not interfere with this pro-metastatic pathway Mus musculus
additional information concept of the protease web as the complex interplay between proteinases, their inhibitors and effector molecules, overview Mus musculus
physiological function uPA is a crucial protagonist for the tissue inhibitor of metalloproteinases-1, TIMP-1, induced modulation of a pro-metastatic microenvironment in the liver of mice. Elevated levels of TIMP-1 render the liver more susceptible to metastasis by triggering urokinase plasminogen activator expression as well as hepatocyte growth factor signalling, thereby leading to the fatal scattered infiltration of metastasizing tumour cells throughout the parenchyma of the target organ. Host uPA is necessary for the recruitment of neutrophilic granulocytes and the associated increase of HGF in livers with elevated TIMP-1 levels Mus musculus
physiological function uPA is a crucial protagonist for the tissue inhibitor of metalloproteinases-1, TIMP-1, induced modulation of a pro-metastatic microenvironment in the liver of mice. Elevated levels of TIMP-1 render the liver more susceptible to metastasis by triggering urokinase plasminogen activator expression as well as hepatocyte growth factor signalling, thereby leading to the fatal scattered infiltration of metastasizing tumour cells throughout the parenchyma of the target organ. Host uPA is necessary for the recruitment of neutrophilic granulocytes and the associated increase of HGF in livers with elevated TIMP-1 levels Homo sapiens